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Increased Intracranial Pressure

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  • 1. INCREASED INTRACRANIAL PRESSURE Ma. Tosca Cybil A. Torres, RN
  • 2.
    • INTRACRANIAL PRESSURE
        • is the pressure exerted by the cranium on the brain tissue, cerebrospinal fluid (CSF), and the brain's circulating blood volume
        • constantly fluctuating in response to activities such as exercise, coughing, straining, arterial pulsation, and respiratory cycle
        • measured in millimeters of mercury (mmHg)
        • at rest, is normally 7–15 mmHg for a supine adult
        • becomes negative (averaging −10 mmHg) in the vertical position
  • 3.
    • Cerebral Dynamics
    • Cerebrospinal Fluid (CSF)
        • a. production
        • produced in choroid plexuses of lateral, third and fourth ventricles
        • produced at rate of 500 cc/day or approximately 20cc/hour
        • eliminated by being absorbed into the arachnoid villi --> dural sinus --> jugular system
        • b. circulation
  • 4.
    • Cerebral Blood Flow (CBF)
          • 750 mL/minute which is 15% of the cardiac output
    • Autoregulation
          • pressure autoregulation
            • arterioles dilate or constrict in response to changes in BP and ICP in order to maintain a constant CBF
  • 5.
    • b. metabolic autoregulation
        • arterioles dilate in response to potent chemicals that are by-products of metabolism such as lactic acid, carbon dioxide and pyruvic acid
            • CO2 is a potent vasodilator
            • increased CO2/decreased BP --> vasodilation
            • decreased CO2/increased BP --> vasoconstriction
  • 6. PATHOPHYSIOLOGY
    • Causes of increased intracranial pressure can be classified by the mechanism in which ICP is increased:
    • mass effect such as brain tumor, infarction with oedema, contusions, subdural or epidural hematoma, or abscess all tend to deform the adjacent brain.
    • generalized brain swelling can occur in ischemic-anoxia states, acute liver failure, hypertensive encephalopathy, pseudotumor cerebri, hypercarbia, and Reye hepatocerebral syndrome. These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts.
    • increase in venous pressure can be due to venous sinus thrombosis, heart failure, or obstruction of superior mediastinal or jugular veins.
    • obstruction to CSF flow and/or absorption can occur in hydrocephalus (blockage in ventricles or subarachnoid space at base of brain, e.g., by Arnold-Chiari malformation), extensive meningeal disease (e.g., infectious, carcinomatous, granulomatous, or hemorrhagic), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption).
  • 7. Elevation in ICP can be graded as follows:   Normal ICP                             0 - 15mm Hg Mile elevation                           16 - 20 mm Hg Moderate elevation                   21 - 30 mm Hg Sever elevation             31 - 40 mm Hg Very severe elevation            41 mm Hg and above   SIGNS AND SYMPTOMS
    • Early Signs
    • decreased level of consciousness, confusion, restlessness, lethargy, difficulty with memory and thinking
    • pupillary dysfunction
    • changes in vision
    • deterioration of motor function
    • Headache, personality changes
    • decreasing Glascow Coma Score
    •  
  • 8.
    • Later Signs
    • continued decrease in level of consciousness (stuporous, comatose)
    • dilated pupils, no reaction to light
    • hemiplegia that progresses
    • vomiting
    • bradycardia
    • hyperthermia
    • papiledema
  • 9.
    • Late changes include:
    •  
    • Decreased LOC with difficulty to arouse and further decrease in the Glascow Coma Score.  More stimulation will be required to elicit any type of response.
    • Pupils will become unilaterally enlarged progressing to fixed and dilated.  Eventually becoming bilaterally fixed and dilated with noted papilledema.
    • Decorticate  or decerebrate posturing to flaccidity will occur.
    • Patient may only posture to painful stimuli.
    • Speech may be absent with only moaning.
    • Respiration will be irregular advancing to Neurogenic hyperventilation and respiratory arrest.
    • Loss of corneal and gag reflexes.
    • Abnormal reflexes such as positive Babinski reflex.
    • Vital signs will present the "Cushing triad".
    • hypertention, bradycardia, widening pulse pressure
  • 10. INTERVENTIONS FOR THE PATIENT WITH INCREASED ICP
    • Goals of Therapy
    • Maintain cerebral perfusion pressure.
    • b. Prevent focal or global cerebral ischemia and focal brain compression
    • Nursing Management includes:
    •  
    • Maintain the patients head midline to facilitate blood flow.
    • Maintain the head of the bed at 30 - 45 degrees to facilitate venous drainage.
    • Avoid activities that can increase ICP such as suctioning or gagging.
    • Treat hyperthermia as it increases the metabolic needs of the brain.
    • Decrease environmental stimuli which can increase ICP.
  • 11.
      • 6. Dim all lights
      • 7.Speak softly
      • 8.Touch gently and only when needed
      • 9. Space all interventions
      • 10. Limit noxious stimuli such as suctioning to only as needed
      • 11. Maintain fluid balance via accurate I & O.  Overhydration will lead to cerebral edema.
      • 12.Monitor electrolytes as these patients are prone to hypernatremia, hypoglycemia, and hypokalemia with diuretic useage.
      • 13. Monitor hyperventilation to maintain CO2 levels at 25 - 35mm Hg to prevent vasodilation.
      •  
    •  
  • 12.
    • Medical Management includes:
    •  
        • Anticonvulsant therapy for seizures.
        • Use of diuretics such as Mannitol, Urea, and Glycerol.
        • Barbiturate Coma Therapy to decrease the metabolic demands of the brain.
        • 50% Dextrose solution if hypoglycemia is present and persistent.
        • 5. Surgical decompression
        • -         considered life saving measure
        • -         opening of the skull can lead to severe herniation
  • 13.
    • Specific Treatment
        • Surgical removal of intracranial masses.
        • b. Placement of extraventricular drain (temporary).
        • c. Placement of VP shunt (usually permanent).
  • 14.
    • b. Fluid Restriction
        • restrict fluids to 65-75% of normal maintenance fluids
        • 2. use 0.9% NS when possible
        • 3. D5W may decrease osmolarity of the blood and increase cerebral edema; may cross BBB and negate effect
    • c. Hypothermia
    • d. Elevation of the Bed
      • 1. raise the head of the bed 25-30 degrees to promote intracranial drainage
      • 2. promotes venous drainage
      • 3. avoid compression of jugular veins or kinking of the neck
  • 15. Pharmacologic Methods
    • Osmotic Diuretics
      • Mannitol
          • MOA: reduces the water content of the brain due to the establishment of an osmotic gradient between the brain and the intravascular compartment. Mannitol is a large molecule and will not cross the BBB.
        •  
          • b. Dosage: 50 – 200 Gm (1 Gm/kg) IV over 24 hours
          •                    Titrated to maintain urine output at 30 – 50cc/hr.
          •           
          • c. Contraindications:
          • Patients with anuria related to renal disease, pulmonary edema, severe dehydration, or active intracranial bleeding.
          • d. Usually used with Lasix 0.5mg/kg.
  • 16.
        • e. Nursing Implications:
            • Assure foley patency
            • Preassessment of patients cardiovascular status
            • Monitor electrolytes frequently : serum and urine osmolarity, serum and urine electrolytes
            • Always use a filtered needle due to crystallization of the drug
            • An administration set with a 0.22 micron filter must be used
            • Available iv as 20% solution (100 gm in 500 ml of d5w)
            • Must be kept warm or will precipitate
            • Adverse effects: chf, pulmonary edema, kidney failure
  • 17.
    • 2. Glycerol
        • MOA: reduces CSF production along with osmotic effects
        • Dose: 0.5 to 1.0 gm/kg Q 4-6 hours; do not exceed 0.2-1.0 gm/kg/hour
        • give IV as a 10-20% solution in 0.45% or 0.9% saline over several hours (3-5 hours)
        • Side Effects: rate-related; reduced with slow infusion
    • Nursing Implications:
          • Slow acting
          • Can be used long-term
          • Metabolized by the body producing energy
          • Mix with iced lemon or juice
          • Monitor electrolytes due to diuresis
  • 18.
    • b. Loop Diuretics- Furosemide, Ethacrynic Acid
        • MOA: inhibit sodium and chloride resbsorption in the loop of Henle resulting in contraction of the blood volume which may mobilize cerebral edema
        • 2. usually administered with mannitol to increase the therapeutic effect
        • 3. Dose: 0.5 to 1.0 mg/kg prn
        • 4. Side Effects: hypokalemia, dehydration, hypotension, glucose intolerance
  • 19.
    • c. Corticosteroids
        • 1. only proven to be effective in reducing cerebral edema associated with brain tumors; role in traumatic cerebral edema is uncertain
        • 2. MOA: exact mechanism unknown; may decrease CSF production and stablize brain cell membranes
        • 3. Dose: dexamethasone most commonly used; 10 mg IV/IM followed by 4 mg IV/IM Q 6 hrs
        • 4. Side Effects: hyperglycemia, GI bleeding, increased infection risk
  • 20.
    • End of discussion